*H-MRS neuroimaging obtains chemical spectra from multiple volume-image elements, or voxels, within the human brain using radiofrequencies that excite protons. (Ross and Sachdev, 2004) Specific molecules are identified by their characteristic resonance frequency in the spectrum. Once acquired, spectra are analyzed to determine the relative concentrations of different molecules or central nervous system metabolites within the voxel or region of interest. Typical metabolites identified are: glutamate (Glu), N-acetyl-aspartate (NAA), creatine (Cr), choline (Cho), lactate, lipid, myoinositol, gamma-aminobutyric acid (GABA), and glutamine (Gln). Glu and GABA are of particular importance to brain neurophysiology as they are components of excitatory and inhibitory neurotransmission, respectively. Glu binds to both ionotropic and metabotropic receptors located on postsynaptic neurons and causes excitability (i.e. depolarization). Moreover changes in the strength of Glu neurotransmission are typically indicative of synaptic plasticity, a process proposed to be involved in chronic pain.(Zhuo, 2008) H-MRS methods display multiple features which are amenable to longitudinal studies. High-resolution anatomical scans can be used to isolate identical brain regions on successive sessions that are even weeks apart. Measurement of metabolites within the central nervous system has been largely understudied in the field of pain. Grachev et al. has reported that the level of NAA, a marker for neuronal viability and also function (Nakano et al., 1998; Sager et al., 2001), is lower within the dorsolateral prefrontal cortex of individuals with chronic low back pain as compared to healthy controls.(Grachev et al., 2000) In addition, a recent investigation has begun to implement H-MRS technology to assess functional changes in the concentrations of Glu in response to evoked pain stimuli.(Mullins et al., 2005) Mullins et al. have observed that Glu levels increase by as much as 10% in the anterior cingulate in response to cold pain applied to the foot. Glu in the central nervous system may play a role in FM pathophysiology. A study by Peres et al. found that cerebrospinal fluid levels of Glu were elevated in FM patients possibly having consequences for glutamatergic neurotransmission.(Peres et al., 2004) Administration of ketamine, a glutamate channel blocker, has been found to reduce experimental pain (Graven-Nielsen et al., 2000) and clinical pain (Cohen et al., 2006) in FM. Moreover our group recently demonstrated that long-term treatment of FM patients with acupuncture can lead to changes in Glu levels within the posterior insula and that these changes are highly correlated with changes in pain: greater reductions in Glu are associated with greater reductions in both experimental and clinical pain (Harris et al., 2008). In addition, we have recently compared posterior insula Glu and combined Glu + Gln (Glx) between FM patients and matched controls and have demonstrated that the patients have elevated Glx (and Glu) levels. (Harris et al., 2009).